Overactive bladder that is one of the diseases leading to a lower urinary tract symptom refers to a clinical condition showing an urinary urgency regardless of the presence or absence of incontinence, which is usually accompanied by a urinary frequency and nocturnal urinary frequency (Non-Patent Document 1). For a treatment of the disease, currently an anticholinergic agent is mainly used, and constant treatment results are given. However, it has been reported that the anticholinergic agent is difficult to be used for patients with prostatic hypertrophy or elderly patients because it is known to cause side-effects such as dry mouth, constipation and blurred vision, as well as a risk of urinary retention. In addition, there are patients showing no improvement with the anticholinergic agent. From the above facts, there is a great expectation about a drug with a new mechanism of action for overactive bladder.
Prostaglandin E2 (PGE2) is a bioactive substance, a precursor of which is arachidonic acid, and is known to participate in regulating functions of the body through 4 subtypes of G-protein coupled receptors, i.e., EP1, EP2, EP3, and EP4.
It has been known that intravesical instillation of PGE2 results in strong urinary urgency and reduction in the bladder capacity in humans (Non-Patent Document 2), and that it results in reduction in the bladder capacity of a rat (Non-Patent Document 3). Accordingly, it has been suggested that there is a possibility that PGE2 influences the function of lower urinary tract. Recently, there has been reported that administration of an EP1 receptor antagonist to a model rat with spinal cord injury is useful in improving the urination function (Non-Patent Document 4), and suggested that the abnormal urination function of a model mouse with urethral stricture is lost in EP1 receptor knock-out mice, and that intravesical instillation of PGE2 shows hyperactivity of the abnormal urination function (Patent Document 1). From these, it is believed that the EP1 receptor antagonist is useful as a remedy for a lower urinary tract symptom.
Moreover, the EP1 receptor antagonist has such a mechanism that particular side effects caused by an anticholinergic agent are expected to be avoided, and an effect on patients whom showed no improvement with the anticholinergic agent is also expected. In addition, this agent is expected to improve certain symptoms further by acting on sensory nerves. Furthermore, this agent has been reported to exhibit an effect of improving clinical condition without lowering the urination efficiency in a model rat with spinal cord injury (Non-Patent Document 5), and thus it is expected to be administered safely to patients with prostatic hypertrophy or elderly patients.
In addition, it has been widely known that PGE2 is produced locally due to inflammation or tissue damage, and enhances the inflammation reaction as well as participating in giving pain or fever. Recently, it has been known that an EP1 receptor antagonist shows efficacy in the model animals with pains of various types such as inflammatory pain (Non-Patent Document 6), postoperative pain (Non-Patent Document 7), and neuropathic pain (Non-Patent Document 8). There is also a report on the clinical effect of administering an EP1 receptor antagonist on visceral pain caused by hydrochloric acid (Non-Patent Document 9). From these, it is believed that the EP1 receptor antagonist is also useful as a remedy for various pains.
Moreover, it has been known that the EP1 receptor antagonist has an inhibitory effect on aberrant crypt foci of the colonic mucosa and on intestinal polyp formation (Patent Document 2), thus it is believed to be useful as a remedy for colon cancer, bladder cancer, prostate cancer, or the like.
As a sulfonamide compound having an EP1 receptor antagonistic activity, for example, compounds mentioned in Patent Documents 3 and 4 have been reported.
Patent Document 3 discloses a compound represented by the formula (A):

(wherein A and B each independently represents a C5 to 15 carbon ring or a 5- to 7-membered heterocycle, Z3 represents a single bond or C1 to 4 alkylene, Z4 represents SO2 or CO, R2 represents an amide bond, —O—Cl to 4 alkylene, or the like, R4 represents (1) hydrogen, (2) C1 to 8 alkyl, C2 to 8 alkenyl, or C2 to 8 alkynyl, (3) C1 to 6 alkyl substituted with 1 or 2 substituents selected from the group consisting of COOZ8, CONZ9Z10, OZ8, and C1 to 4 alkoxy, (4) C3 to 7 cycloalkyl, or (5) C1 to 4 alkyl, C2 to 4 alkenyl, or C2 to 4 alkynyl, each of which substituted with phenyl or C3 to 7 cycloalkyl, and further, Z8, Z9, and Z10 each independently represents hydrogen or C1 to 4 alkyl. For the other symbols, reference can be made to the publication.)
However, there is no specific disclosure of the active ingredient represented by the formula (I) that is an active ingredient of the present invention.
Further, Patent Document 4 discloses a compound represented by the formula (B).

(wherein R5 represents isopropyl, isobutyl, 2-methyl-2-propenyl, cyclopropyl methyl, methyl, ethyl, propyl, 2-propenyl, or 2-hydroxy-2-methyl propyl. As the other symbols, reference can be made to the publication.)
However, it has a basic structure different from that of the active ingredient represented by the formula (I) that is an active ingredient of the present invention, since R5 has no amide structure.
In addition, as the sulfonamide compound, for example, compounds mentioned in Patent Documents 5 to 8 have been reported.
Patent Document 5 discloses that a compound represented by the formula (C) including a wide variety of compounds has an inhibitory activity against the production of an amyloid β protein, and is useful for treating or preventing Alzheimer's disease, or the like.

(for the symbols in the formula, see the publication)
However, there is no description on an EP1 receptor antagonistic activity of the compound, and also no specific disclosure of the compound (II) of the present invention.
Moreover, Patent Document 6 discloses that a compound represented by the formula (D) including a wide variety of compounds has farnesoid-X receptor (FXR) antagonistic activity, and is useful for treating diseases related to cholesterol abnormality, obesity, diabetes, or the like.[Chem. 4]B1-L1-A1-L2-B2  (D)
(for the symbols in the formula, see the publication)
However, there is no description on an EP1 receptor antagonistic activity of the compound, and also no specific disclosure of the compound (II) of the present invention.
Furthermore, Patent Document 7 discloses that a compound represented by the formula (E) has orexin receptor antagonistic activity, and is useful for treating sleep disorders, stress-related disorders, or the like.

(for the symbols in the formula, see the publication)
However, there is no description on an EP1 receptor antagonistic activity of the compound, and also no specific disclosure of the compound (II) of the present invention.
Furthermore, Patent Document 8 discloses that a compound represented by the formula (F) has diacylglycerol acyl transferase (DGAT) inhibitory activity, and is useful for treating or preventing obesity, hyperlipidemia, diabetes, or the like.

(for the symbols in the formula, see the publication)
However, there is no description on an EP1 receptor antagonistic activity of the compound, and also no specific disclosure of the compound (II) of the present invention.
In addition, methyl 4-({[N-[(4-fluorophenyl)sulfonyl]-N-(2-methoxyphenyl)glycyl]amino}methyl)benzoate (Registry Number: 851172-09-3; for example, Catalogue name: Aurora Screening Library, Order No. kend-0100022), and N2-[(4-chlorophenyl)sulfonyl]-N2-(2,5-difluorophenyl)-N-[4-(1,2,3-thiadiazol-4-yl)benzyl]-D-alaninamide (Patent Document 5, Example 635) having amyloid β protein-production inhibitory activity have been known.
However, there are no reports on the EP1 receptor antagonistic activity of these compounds.
[Non-Patent Document 1] “Neurourology and Urodynamics”, (England), 2002, Vol. 21, p. 167-78
[Non-Patent Document 2] “Urological Research”, (USA), 1990, Vol. 18, No. 5, p.
[Non-Patent Document 3] “The Journal of Urology”, (USA), June 1995, Vol. 153, No. 6, p. 2034-8
[Non-Patent Document 4] “Journal of The Japanese Urological Association”, February 2001, Vol. 92, No. 2, p. 304
[Non-Patent Document 5] “The 89th Annual Meeting of The Japanese Urological Association”, Kobe, 2001, MP-305
[Non-Patent Document 6] “Anesthesiology”, (USA), November 2002, Vol. 97, No. 5, p. 1254-62
[Non-Patent Document 7] “Anesthesia and Analgesia”, (USA), December 2002, Vol. 95, No. 6, p. 1708-12
[Non-Patent Document 8] “Anesthesia and Analgesia”, (USA), October 2001, Vol. 93, No. 4, p. 1012-7
[Non-Patent Document 9] “Gastroenterology”, January 2003, Vol. 124, No. 1, p.
[Patent Document 1] US2005/0020646
[Patent Document 2] WO00/069465
[Patent Document 3] WO98/027053
[Patent Document 4] WO02/072564
[Patent Document 5] WO 00/050391
[Patent Document 6] WO 02/020463
[Patent Document 7] WO 04/033418
[Patent Document 8] Japanese Patent Application Publication No. 2005-206492